Environmental variation of arsenic levels in human blood determined by neutron activation analysis

Heydorn, Κ.

doi:10.1016/0009-8981(70)90101-4

Cited by 72 publications

(21 citation statements)

References 3 publications

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“…It has been reported that arsenic concentrations in red blood cells of residents exposed to arsenic from drinking water in Taiwan and Blackfoot prevalent areas could reach 1.2 and 15 mM, respectively 12) . We used this range of arsenic concentrations to treat human cells to examine the effect of arsenic on DNA integrity, and found that arsenic significantly induced DNA strand breaks in a dose-dependent manner in HL60 and mononucleocytes, respectively.…”

Section: Discussionmentioning

confidence: 99%

Arsenic induces DNA damage via reactive oxygen species in human cells

Morimoto

Takeshita

et al. 2001

Environ Health Prev Med

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To elucidate arsenic-induced oxidative DNA damage, the genotoxicity of arsenic in human cells was comparatively studied with single cell gel electrophoresis (SCGE) assay in combination with the observation of the protective effects of dimethyl sulfoxide (DMSO) and catalase. Arsenic, at the concentration of 2.4 mM by coincubation for 24 hours, significantly induced DNA damage in HL60, a human promyelocytic leukemia cell line. In contrast, significant DNA damage was found in human mononucleocytes at the concentration of 4.8 mM or above. The cells were incubated separately with DMSO (12 mM/l), a well-known hydroxyl radical (OH ----) scavenger, and catalase (1,300 U/ml), a hydrogen peroxide (H 2 O 2 ) scavenger, for 6 hours and then further coincubated with various concentrations of arsenic for 24 hours at 37°°°°C and 5% CO 2 . The findings showed that both DMSO and catalase significantly reduced the arsenic-induced tail moment, a parameter of total damaged DNA, in HL60 and mononucleocytes. Hence our findings indicate that arsenic, with micromolar concentrations, induces typical and various extents of DNA damage in human cells via reactive oxygen species in a dose-dependent manner.

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Section: Discussionmentioning

confidence: 99%

Arsenic induces DNA damage via reactive oxygen species in human cells

Morimoto

Takeshita

et al. 2001

Environ Health Prev Med

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“…Aliquots were taken for the ordinary (iron, zinc and copper) and hydride (arsenic and selenium) modes of the atomic absorption spectrophotometer (20)(21)(22)(23)(24) 21 10 Results and Discussion…”

Section: Methodsmentioning

confidence: 99%

Studies on the Concentrations of Arsenic, Selenium, Copper, Zinc and Iron in the Hair of Blackfoot Disease Patients in Different Clinical Stages

Wang¹,

Chang²,

Huang³

et al. 1994

CCLM

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Summary:Flame atotnic absoφtion spectrophotometric methods were developed for, arsenic, selenium, copper, zinc and iron in hair samples. Data from blackfoot disease patients at five clinical stages were compared with those from healthy controls. The copper and zinc concentrations showed only slight differences in all clinical stages, which indicated the less relation to blackfoot disease.The decrease of selenium and iron in all stages was attributed to the antagonistic effect of arsenic; arsenic increased in the first and second stages, but decreased in the later stages. The decrease of selenium and iron during the Progression of the disease is thought to be due to persistence of the antagonistic effect of arsenic in the initial stages, so that very low concentrations of selenium are found in the advanced stages, despite the later decrease of arsenic. There was also a progressive decrease of iron with advance of the disease, and the later stages also showed a decrease in haemoglobin.It was shown that arsenic is a major cause of blackfoot disease, and that it antagonises selenium and iron, which decreased in the advanced clinical stages of the disease.

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“…Although arsenite (20 to 80 mol/L) 12 and methylated arsenic (at mmol/L level) 13 have been reported to induce DNA strand breaks in cultured mammalian cells, the involvement of arsenic-induced DNA damage in human disorders is somewhat unconvincing, because the concentrations of arsenic used were beyond the range of normal exposure. In Blackfoot disease-affected areas of Taiwan, arsenic concentrations in drinking water and in red blood cells of residents 14 can reach 15 and 1.2 mol/L, respectively. Therefore, we examined the effect of arsenite at 1 to 10 mol/L levels on DNA integrity of human VSMCs.…”

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confidence: 99%

NADH Oxidase Activation Is Involved in Arsenite-Induced Oxidative DNA Damage in Human Vascular Smooth Muscle Cells

Lynn

Gurr

Lai

et al. 2000

Circulation Research

279

137

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Abstract-Arsenic is atherogenic, carcinogenic, and genotoxic. Because atherosclerotic plaque has been considered a benign smooth muscle cell tumor, we have studied the effects of arsenite on DNA integrity of human vascular smooth muscle cells. By using single-cell alkaline electrophoresis, apparent DNA strand breaks were detected in a 4-hour treatment with arsenite at a concentration above 1 mol/L. DNA strand breaks of arsenite-treated cells were increased by Escherichia coli formamidopyrimidine-DNA glycosylase and decreased by diphenylene iodinium, superoxide dismutase, catalase, pyruvate, DMSO, or D-mannitol. Extract from arsenite-treated cells showed increased capacity for producing superoxide when NADH was included in the reaction mixture; however, addition of arsenite to extract from untreated cells did not increase superoxide production. The superoxide-producing ability of arsenite-treated cells was also suppressed by diphenylene iodinium, 4,5-dihydroxy-1,2-benzenedisulfonic acid disodium salt (Tiron), or superoxide dismutase. Superoxide production and DNA strand breaks in arsenite-treated cells were also suppressed by transfecting antisense oligonucleotides of p22phox, an essential component of NADH oxidase. Treatment with arsenite also increased the mRNA level of p22phox. These results suggest that arsenite activates NADH oxidase to produce superoxide, which then causes oxidative DNA damage. The result that arsenite at low concentrations increases oxidant levels and causes oxidative DNA damage in vascular smooth muscle cells may be important in arsenic-induced atherosclerosis. (Circ Res. 2000;86:514-519.)Key Words: arsenite Ⅲ oxidative DNA damage Ⅲ NADH oxidase Ⅲ atherosclerosis A rsenic, an element present in the earth's crust, comes to the surface through mining and utilization of groundwater. Serious contamination by inorganic arsenic occurs through long-term ingestion of high concentrations of arsenic in drinking water. Chronic exposure to arsenic has been related to increased incidences of skin, lung, bladder, liver, and kidney cancers. 1,2 Arsenic exposure is also associated with various vascular disorders, including angiosarcomas, 3 atherosclerotic plaques, 4 and hypertension in humans. 5 The epidemiological evidence for shared risk factors for cancer and atherosclerosis has been reviewed by Hansen. 6 Exposure to carcinogenic environmental agents is associated with an increased risk of atherosclerosis. Therefore, somatic mutation and cell proliferation may play a role in the pathogenesis of atherosclerotic plaques. The predominant cell type in plaques is the vascular smooth muscle cell (VSMC). Proliferation of VSMCs is essential for plaque formation and development. By examining the isoenzymes of glucose-6-phosphate dehydrogenase, human atherosclerotic plaques were shown to be monoclonal in origin. 7 Furthermore, DNA samples from human coronary artery plaques were demonstrated to transform NIH3T3 cells. 8 These observations suggest that atherosclerotic plaques are presumably benign smooth muscle...

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Environmental variation of arsenic levels in human blood determined by neutron activation analysis

Cited by 72 publications

References 3 publications

Arsenic induces DNA damage via reactive oxygen species in human cells

Arsenic induces DNA damage via reactive oxygen species in human cells

Studies on the Concentrations of Arsenic, Selenium, Copper, Zinc and Iron in the Hair of Blackfoot Disease Patients in Different Clinical Stages

NADH Oxidase Activation Is Involved in Arsenite-Induced Oxidative DNA Damage in Human Vascular Smooth Muscle Cells

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